Evidence map›Paper›PMID 31078518›Full record

ArticleEBioMedicine2019

Seno-destructive smooth muscle cells in the ascending aorta of patients with bicuspid aortic valve disease.

Brittany Balint, Hao Yin, Zengxuan Nong, John-Michael Arpino, Caroline O'Neil, Stephanie R Rogers, Varinder K Randhawa, Stephanie A Fox, Jacqueline Chevalier, Jason J Lee and 2 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in EBioMedicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
4.2field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

31 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
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  9. Endothelial-to-Mesenchymal Transition in Cardiovascular Pathophysiology.International journal of molecular sciences · 2024
    Review
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  14. Telomere Length: Implications for Atherogenesis.Current atherosclerosis reports · 2023
    Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors at 1 institution in 1 country.

Brittany BalintRobarts Research Institute, The University of Western Ontario, 1151 Richmond St. N., London, ON N6A 5B7, Canada; Department of Medical Biophysics, The University of Western Ontario, 1151 Richmond St. N., London, ON N6A 5C1, Canada.
Hao YinRobarts Research Institute, The University of Western Ontario, 1151 Richmond St. N., London, ON N6A 5B7, Canada.
Zengxuan NongRobarts Research Institute, The University of Western Ontario, 1151 Richmond St. N., London, ON N6A 5B7, Canada.
John-Michael ArpinoRobarts Research Institute, The University of Western Ontario, 1151 Richmond St. N., London, ON N6A 5B7, Canada; Department of Medical Biophysics, The University of Western Ontario, 1151 Richmond St. N., London, ON N6A 5C1, Canada.
Caroline O'NeilRobarts Research Institute, The University of Western Ontario, 1151 Richmond St. N., London, ON N6A 5B7, Canada.
Stephanie R RogersRobarts Research Institute, The University of Western Ontario, 1151 Richmond St. N., London, ON N6A 5B7, Canada.
Varinder K RandhawaDepartments of Medicine (Cardiology), The University of Western Ontario, 1151 Richmond St. N., London, ON N6A 5C1, Canada.
Stephanie A FoxDepartment of Surgery, The University of Western Ontario, 1151 Richmond St. N., London, ON N6A 5C1, Canada; London Health Sciences Centre, 339 Windermere Rd., London, ON N6A 5A5, Canada.
Jacqueline ChevalierRobarts Research Institute, The University of Western Ontario, 1151 Richmond St. N., London, ON N6A 5B7, Canada; Department of Medical Biophysics, The University of Western Ontario, 1151 Richmond St. N., London, ON N6A 5C1, Canada.
Jason J LeeRobarts Research Institute, The University of Western Ontario, 1151 Richmond St. N., London, ON N6A 5B7, Canada; Department of Medical Biophysics, The University of Western Ontario, 1151 Richmond St. N., London, ON N6A 5C1, Canada.
Michael W A ChuDepartment of Surgery, The University of Western Ontario, 1151 Richmond St. N., London, ON N6A 5C1, Canada; London Health Sciences Centre, 339 Windermere Rd., London, ON N6A 5A5, Canada.
J Geoffrey PickeringRobarts Research Institute, The University of Western Ontario, 1151 Richmond St. N., London, ON N6A 5B7, Canada; Department of Medical Biophysics, The University of Western Ontario, 1151 Richmond St. N., London, ON N6A 5C1, Canada; Departments of Medicine (Cardiology), The University of Western Ontario, 1151 Richmond St. N., London, ON N6A 5C1, Canada; London Health Sciences Centre, 339 Windermere Rd., London, ON N6A 5A5, Canada; Department of Biochemistry, The University of Western Ontario, 1151 Richmond St. N., London, ON N6A 5C1, Canada. Electronic address: gpickering@robarts.ca.
Western University · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAscending aortic aneurysms constitute an important hazard for individuals with a bicuspid aortic valve (BAV). However, the processes that degrade the aortic wall in BAV disease remain poorly understood.

methodsWe undertook in situ analysis of ascending aortas from 68 patients, seeking potentially damaging cellular senescence cascades. Aortas were assessed for senescence-associated-ß-galactosidase activity, p16

findingsWe uncovered SMCs at varying depths of cellular senescence within BAV- and tricuspid aortic valve (TAV)-associated aortic aneurysms. Senescent SMCs were also abundant in non-aneurysmal BAV aortas but not in non-aneurysmal TAV aortas. Multivariable analysis revealed that BAV disease independently associated with SMC senescence. Furthermore, SMC senescence was heightened at the convexity of aortas associated with right-left coronary cusp fusion. Aged BAV SMCs had a pronounced collagenolytic SASP. Moreover, senescent SMCs in the aortic wall were enriched with surface-localized MMP1 and surrounded by weakly birefringent collagen fibrils. The senescent-collagenolytic SMC phenotype depended on p38 MAPK signaling, which was chronically activated in BAV aortas.

interpretationWe have identified a cellular senescence-collagen destruction axis in at-risk ascending aortas. This novel "seno-destructive" SMC phenotype could open new opportunities for managing BAV aortopathy. FUND: Canadian Institutes of Health Research, Lawson Health Research Institute, Heart and Stroke Foundation of Ontario/Barnett-Ivey Chair.

Indexed as

AgedAged, 80 and overAortaAortic AneurysmAortic ValveBicuspid Aortic Valve DiseaseBiomarkersCells, CulturedCellular SenescenceCollagenDNA Breaks, Double-StrandedFemaleHeart Valve DiseasesHumansImmunohistochemistryMiddle AgedBiomarkersCollagenAortic aneurysmBicuspid aortic valveCellular senescenceCollagenaseSmooth muscle cells

Identifiers

PMID31078518
PMCPMC6562112
OpenAlexW2944583173

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.